Drug-induced oedema

Summary

Besides more classical aetiologies for oedema such as heart failure, liver cirrhosis, nephrotic syndrome and chronic venous insufficiency, in practice we increasingly observe iatrogenic or drug-induced oedema as adverse events. Many drugs have the potential to cause oedema or to worsen pre-existing oedema prior to the initiation of drug therapy. Drug-induced oedema is frequently caused by calciumchannel-blockers of the dihydropyridine-type but can also be caused by dihydralazine and minoxidil which are less frequently prescribed. Other drugs which may support the formation of oedema are diuretics, nonsteroidal anti-inflammatory drugs (NSAIDs), ACE-inhibitors or AT₁-receptor-antagonists (angioedema) and thiazolidinediones/glitazones which are used as oral anti-diabetics.

This review focuses on drug-induced oedema, pathophysiological considerations and potential treatment and management strategies from a clinical-pharmacological perspective.

Zusammenfassung

Neben den ätiologisch klassischen Ödemkrankheiten Herzinsuffizienz, Leberzirrhose, nephrotisches Syndrom und der chronischen venösen Insuffizienz werden klinisch zunehmend auch iatrogene und medikamentös induzierte Ödeme in der Praxis beobachtet. Verschiedene Arzneimittel können klassen- bzw. wirkstoffspezifisch Ödeme verursachen oder bestehende Ödeme verschlechtern. Am häufigsten sind direkte Vasodilatoren und hier in erster Linie Kalziumantagonisten der Dihydropyridingruppe ursächlich in Betracht zu ziehen, aber auch Dihydralazin und Minoxidil, die jedoch selten verordnet werden. Weitere Arzneimittel, die zu einer Ödembildung führen können, sind Diuretika, nicht steroidale Antiphlogistika, ACE-Hemmer und AT₁-Rezeptor-blocker (Angioödeme) sowie die Gruppe der antidiabetisch wirksamen Thiazolidindione-/Glitazone.

Dieser Übersichtsartikel fokussiert auf Arzneimittel als mögliche Ödemauslöser und fasst die wichtigsten mit einer Ödembildung als unerwünschter Arzneimittelwirkung (UAW) assoziierten Medikamente, die zugrunde liegenden Pathomechanismen und mögliche Behandlungsstrategien aus klinisch-pharmakologischer Sicht zusammen.

Résumé

En dehors des étiologies plus habituelles des œdèmes telles que l’insuffisance cardiaque, la cirrhose hépatique, le syndrome néphrotique et l’insuffisance veineuse chronique, on observe de manière croissante des œdèmes iatrogènes ou constituant des effets secondaires d’origine médicamenteuse. L’œdème induit par des médicaments de type dihydropyrine est fréquemment causé par le blocage des canaux de calcium mais cela peut également survenir avec la dihydralazine et le minoxidil, de prescription fréquente. D’autres substances qui peuvent accentuer la formation de l’œdème sont les diurétiques, les anti-inflammatoires non stéroïdiens (AINS), les IEC, ou les antagonistes des récepteurs AT₁ (angioœdème) ainsi que les thiazolidinediones / glitazones utilisés en tant qu’antidiabétiques oraux.

Cet article concerne l’œdème induit par les médicaments, des considérations pathophysiologiques et le traitement possible ainsi que la manière de corriger la situation sous une perspective pharmaco-clinique.

Keywords

Drug-induced oedema - vasodilators - calcium channel blockers - loop-diuretics - ACE-inhibitors - AT₁-receptor-blockers - glitazones - pathophysiology - treatment strategies

Schlüsselwörter

Arzneimittelinduzierte Ödeme - Vasodilatoren - Kalziumantagonisten - Schleifendiuretika - ACE-Hemmer - AT₁-Blocker - Glitazone - Pathomechanismen - Behandlungsstrategien

Mots clés

Œdème d’origine médicamenteuse - vasodilatateurs - blocages des canaux de calcium - diurétiques de l’anse - inhibiteurs de l’enzyme de conversion (IEC) - bloqueurs des récepteurs AT₁ - glitazones - pathophysiologie - stratégie thérapeutique

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